The main thrust of the laboratory is focused on the molecular mechanism of platelet aggregation, including both homeostasis and thrombosis. We are investigating the influence of pressure on the hydration layer surrounding the electrically charged amino acid residues involved in platelet aggregation. We have been investigating the molecular mechanism of platelet interactions in DIPA (Decompression-inducible platelet aggregation) for the past several years. We have found tat oppositely charged amino acid residues, i.e., positively charged arginyl and negatively charged aspartyl residues interact with their respective receptor sites. We have observed vascular occlusion in the small blood vessels in the web of the frog's foot and in the ear of the mouse. During the current year we have confirmed that the volume of human PRP is increased by 0.3% or 3 ml per liter of packed thrombocyte volume when platelet aggregation is induced by decompression. A similar volume increase has been observed when platelet aggregation is induced by the agonists, epinephrine (adrenalin), ADP, collagen and PAF (platelet activating factor). We theorize that compactly organized water molecules, when randomized into bulk phase, acquire thermal motion which causes a temperature drop; and the human platelet aggregation is an entropy driven process similar to human red cell sickling. To confirm our hypothesis, we are continuing our experiments with a specially designed dilatometer including a thermistor, to measure the volume increase and temperature drop when platelet aggregation is induced by the agonists epinephrine, ADP, PAF. During the current year we have obtained additional confirmation of volume increase of human plasma due to decompression by using the discontinuous, density gradient zonal centrifugation method.